• Can occur in babies as well as adults and adolescents.

• 3 - 12% of the population have it; it's common.

• Comes in seborrheic distribution - i.e hairy areas.

• (scalp, eye brows, peri nasal folds, chest, sub mammary, axillary, peri umbilical, pubic areas)
  If severe seborrheic dermatitis, think if immunosuppresion -> HIV
  Aetiology unknown -
  Otitis externa and blepharitis (crusty eye lids + occular burning / dryness) are common complications of seborrheic dermatitis. - [Source]PassMedicine

Aetiology: incompletely understood; malazzesia proliferation may play a role along with many other risk factors.

Can be divided into the following:

1. Combined hyperlipidaemia

   1. commonest type of disorder
   2. FCHL - very common (==1/200==) (familial combined hyperlipidaemia)
      1. phenotype: ↑ TGL +/- ↑ LDL-c + suppression of HDL
      2. It is diagnosed by finding raised cholesterol and triglyceride concentrations in association with a typical family history. No physical signs.
      3. Note that familial doesn't mean monogenic.
   3. Remnant hyperilidaemia - another cause of combined hyperlipidaemia:
      1. Patients have increased IDL remnants.
      2. Extreme cardiovasular risk
      3. Pathognomonic physical signs: palmar xanthomata a dn tuberose xanthomata (over knees and elbows)

2. Disorders of chylomicrons and VLDL -
   2. commonest - polygenic hypertriglyceridaemia. ("vast majority" of hypertriglyceridaemia patients are polygenic.) Patients have modest elevations in triglycerides.
   1. Rarely, severe hypertriglyceridemia is caused by monogenic inheritance. (but not necessarily autosomal dominant)

   3. lipoprotein lipase deficiencies - accumulation of chylomicrons in blood -> massive hyperlipidaemia (can see lipid layer in serum samples)
      1. mnemonic; two Ls in lipoprotein lipase and two Ls in lipid layer

3. disorders of LDL -
   2. Heterozygous familial hypercholesterolaemia (HeFH) -
   1. #autosomalDominant
   2. Defective LDL receptor
   3. mild to severe lipid derangement (==1/350== incidence)
   4. Mutations mainly affect the LDLR receptor.
   5. Can have physical signs including xanthomas.

   3. Homozygous familial hypercholesterolaemia (HoFH) - HUGELY elevated LDL-C (==1/250,000== incidence). Most die of ischemic heart disease by age 35

      1. Presents in children.
      2. Also caused by defective LDL receptor.
      3. Poor response to statins.
      4. Liver transplantation can normalize lipid levels. (?introduces hepatocytes with functioning LDL receptors)

   4. Mutations in the apoB and PCSK9 genes - same presentation as HeFH, but milder. Only way to differentiate it genetic tests. - relatively common

   5. Polygenic hypercholesterolaemia - no single identifiable gene deffect but have moderately elevated cholesterol levels.

4. disorders of HDL - rare

See [[passMedicine Summaries#Evaluation of gradual visual loss]]

[!TIP] Mnemonic: RIFC: retina - ipsi, Field - contra

• A particular side of the retina is innervated by the same side of the brain.

• This means that a side of the visual field is connected to the contralateral side of the brain

See also:

• [[opticRadiation1.jpeg]]
• [[opticRadiation3.jpg]]

[!INFO] Retrochiasmal lesions will cause contralateral homonymous visual field defects.
According to the figure above, temporal lobe lesions will cause a contralateral superior quadrantonopia.
These are "Meyer's loop" lesions.

| Hyphema | Retinal detachment |

Evaluation of gradual visual loss

[!INFO] Visual loss means loss of one or more of

• acuity
• Color vision
• visual field

Pearls

• Improvement of acuity with pin hole indicates uncorrected refractive error.
• Occular pathologies and prechiasmal optic neuropathies cause monocular vision loss.
• Amaurosis fugax also presents as transient monocular vision loss.
  • Consider AF as an omen of a stroke
• monocular vision loss is usually due to ocular or pre-chiasmal lesions.
  • Ocular pathologies (corneal, lenticular, vitreoretinal and macular) and prechiasmal optic neuropathies typically cause monocular vision loss.
• Binocular vision loss is usually due to retrochiasmal lesions.
  • In this case, assessment of visual fields can localize the lesions.
  • eg: temporal lobe Meyer's loop leions -> Superior homonymous quadrantonopia.
• most retinal causes of vision loss are painless
• Retrochiasmal lesions will cause contralateral homonymous visual field defects.

Central Vs. Peripheral vision loss:

• Poor central vision with peripheral sparing = macular involvement.
  • eg AMD
  • Manifests as distortions or paracentral scotoma.
• Constricted peripheral vision is usually caused by optic neuropathy.
  • eg: Chronic glaucoma
  • but there are also retinal causes of tunnel vision.
    • eg: retinitis pigmentosa

Speed of onset

• Vascular - rapid.
• Inflammatory - subacute (over days) (eg. optic neuritis, scleritis)
• Degenerative - gradual (cataract)

Leading causes of blindness

• Cataract
• Glaucoma
• Refractive error
• Age-related macular degeneration (AMD)
• Diabetic retinopathy

Retinal vessel occlusion

Source